When functioning properly, a heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout a circulatory system. This intrinsic rhythm is a function of intrinsic signals generated by the sinoatrial node, or SA node, located in the upper right atrium. The SA node periodically depolarizes, which in turn causes the atrial heart tissue to depolarize such that right and left atria contract as the depolarization travels through the atrial heart tissue. The atrial depolarization signal is also received by the atrioventricular node, or AV node, which, in turn, triggers a subsequent ventricular depolarization signal that travels through and depolarizes the ventricular heart tissue causing the right and left ventricles to contract.
Some patients, however, have irregular cardiac rhythms, referred to as cardiac arrhythmias. Cardiac arrhythmias result in diminished blood circulation because of diminished cardiac output. Atrial fibrillation is a common cardiac arrhythmia that reduces the pumping efficiency of the heart. Atrial fibrillation is characterized by rapid, irregular, uncoordinated depolarizations of the atria. These depolarizations may not originate from the SA node, but may instead originate from an arrhythmogenic substrate, such as an ectopic focus, within the atrial heart tissue. The reduced pumping efficiency due to atrial fibrillation requires the ventricle to work harder, which is particularly undesirable in sick patients that cannot tolerate additional stresses. As a result of atrial fibrillation, patients must typically limit activity and exercise.
An even more serious problem, however, is the risk that atrial fibrillation may induce irregular ventricular heart rhythms. Irregular atrial depolarization signals associated with atrial fibrillation are received by the AV node and may be conducted to ventricles. During atrial fibrillation, the intervals between ventricular depolarizations vary substantially. Such induced ventricular arrhythmias compromise pumping efficiency even more drastically than atrial arrhythmias and, in some instances, may be life threatening. This phenomenon is referred to as conducted atrial fibrillation, or “conducted AF.”
A possible explanation for the effect of conducted atrial fibrillation on ventricular rate stability has been suggested. It has been suggested that, during atrial fibrillation, the AV node receives numerous successive stimuli originating from the atrium, and while each stimulus alone has a low amplitude which is insufficient to trigger AV node depolarization and ventricular contraction, they do cause partial depolarizations of the AV node. It has been further suggested that the effect of these partial depolarizations is cumulative, so that when a sufficient number of such stimuli are received, the AV node is depolarized resulting in unstable random ventricular contractions.
One mode of treating cardiac arrhythmias includes the use of an implantable medical device, such as a pacemaker. Pacemakers deliver timed sequences of low energy electrical stimuli, referred to as pacing pulses, to the heart. The pacing pulses cause the cardiac muscle tissue to depolarize, which in turn causes the heart to contract. By properly timing the delivery of pacing pulses, the heart can be induced to contract in proper rhythm, greatly improving its efficiency as a pump.
Wittkampf, F. H. M., et al., “Rate Stabilization by Right Ventricular Pacing in Patients with Atrial Fibrillation,” PACE, Vol. 9, November-December, Part II, 1986, pp. 1147–53, disclosed that during atrial fibrillation, the ventricle can be stabilized by pacing at a rate approximately equal to the average intrinsic ventricular rate. Such therapy improves cardiac output because it stabilizes the rate of ventricular contractions to avoid short periods between contraction, which do not allow adequate ventricular filling, and long periods without a contraction, which lead to a lower average heart rate. The mechanism whereby the ventricular rate is stabilized by a pacing rate lower than the maximal intrinsic ventricular rate is not completely understood. It has been suggested that pacing the ventricles regularizes the ventricular heart rate by establishing retrograde conduction from the ventricles. This, in turn, is believed to block forward conduction of atrial signals through the AV node. As a result, irregular atrial depolarization signals do not trigger resulting irregular ventricular contractions.
In some modes of pacemaker operation, the ventricular pacing rate is defined by a ventricular escape interval. After a paced or intrinsic ventricular depolarization, the pacemaker operating in these modes senses the electrical activity within the ventricle during the escape interval, which is defined from the time of the last paced or intrinsic depolarization, and waits for an intrinsic depolarization to occur. If an intrinsic depolarization does not occur during the escape interval, the pacemaker delivers a pacing pulse.
Methods to stabilize the ventricular rate during conducted atrial fibrillation by pacing at a rate approximately equal to the average intrinsic ventricular rate are known in the art. In realization that the average intrinsic ventricular rate and the ventricular rate stability vary, some existing methods adjust the pacing rate based on changes in the intrinsic ventricular rate or the measured ventricular instability. These existing methods may adjust the pacing rate by adjusting the length of the escape interval of a pacemaker.
Some of the existing methods that adjust the pacing rate based on changes in the intrinsic ventricular rate or the measured ventricular instability, however, are susceptible to over or under pacing caused by rapid changes in the intrinsic ventricular rate. In particular, bursts of rapid intrinsic ventricular depolarizations may lead some existing methods to pace at an undesirably high a rate. Further, some of these existing methods may be slow in reaching a pacing rate that stabilizes the ventricle. Additionally, some of these existing methods may require a complex determination of the stability of the ventricular rate, which may increase the complexity, expense, and power consumption of an implantable device designed to practice the method.
The ventricular cycle length, i.e., the period between ventricular contractions, normally remains relatively constant and varies only gradually, even upon commencement of strenuous exercise. However, occasionally a premature ventricular contraction, or PVC, occurs in the form of a spurious pulse from a muscle cell which alters the normal electrical pulse pattern in the heart. Because the heart tissue does not recover from an early beat in time to conduct the next regular electrical pulse, the subsequent normal heartbeat does not occur. This phenomenon may also be caused by retrograde conduction of the PVC to the AV node, which increases the conduction time of the next regular electrical pulse from the atria. This longer than normal period between ventricular contractions caused by a PVC is referred to as the compensatory pause.
Another existing method for stabilizing the ventricular rate discloses that the length of a compensatory pause can be used as an indicator of the optimal pacing rate for ventricular rate stabilization. Mazzocca, et al., “The Compensatory Pause (CP) of Atrial Fibrillation (AF): A Marker for Ventricular Rate Stabilisation (VRS) in Patients (PTS) with Chronic AF (CAF),” Europace Supplements, Vol. 2, January 2001, p. 21, discloses that the length of a compensatory pause may be measured as the interval between a paced ventricular depolarization and an intrinsic ventricular depolarization. Mazzocca, et al. discloses measuring the length of several compensatory pauses to determine a mean compensatory pause length, and pacing at the rate corresponding to the mean compensatory pause length to stabilize the ventricular rate without significantly increasing the mean ventricular rate.
One existing method to further distinguish paced ventricular depolarizations from intrinsic ventricular depolarizations involves distinguishing between a true paced depolarization and a fusion beat. A fusion beat was not caused by the pacing pulse, but was instead an intrinsic ventricular depolarization that occurred nearly simultaneously with the delivery of the pacing pulse. Fusion beats can result in magnification, diminishment or abolition of the R-wave of the sensed voltage signal. Existing methods determine whether a particular heart depolarization is the result of a fusion beat by examining the T-wave generated during the cardiac cycle containing the particular heart depolarization. A T-wave represents the repolarization of the ventricular tissue and always follows a depolarization of the ventricular tissue. For example, U.S. Pat. No. 5,534,016, issued to Boute, discloses measuring the amplitude of a T-wave to determine whether a particular depolarization was the result of a fusion beat.
Examples of the above referenced existing techniques and/or devices for stabilizing the ventricular rate and for detecting fusion beats may be found in the issued U.S. Patents listed in Table 1 below.
TABLE 1Pat. No.InventorIssue Date6,324,427FlorioNov. 27, 20016,285,907Kramer et al.Sep. 4, 20015,792,193StoopAug. 11, 19985,534,016BouteJul. 9, 19965,480,413Greenhut et al.Jan. 2, 1996
All patents listed in Table 1 above are hereby incorporated by reference herein in their respective entireties. As those of ordinary skill in the art will appreciate readily upon reading the Summary of the Invention, Detailed Description of the Preferred Embodiments and claims set forth below, many of the devices and methods disclosed in the patents of Table 1 may be modified advantageously by using the techniques of the present invention.